Cardiac MRI is able to visualize induced ablation lesions after PVI and might be suitable to quantify ablation lesion amount. Ablation lesion formation did not differ significantly in patients treated with the CB-S vs. the CB-A, despite a significantly lower rate of AF recurrence after 3 months in the CB-A group. Left PVs showed a significantly higher amount of ablation lesions compared with the right PVs. Larger and randomized studies are needed to understand the relationship between representable tissue lesions and success rates.

Background and purpose Left atrial (LA) cardiac disease is a suspected cause of embolic stroke of undetermined source (ESUS). We tested the hypothesis that LA fibrosis, quantified using late‐gadolinium‐enhancement magnetic resonance imaging (LGE‐MRI), predicts recurrent stroke or atrial fibrillation (AF) in patients with ESUS. Methods We compared atrial fibrosis in healthy controls and patients with lacunar stroke, ESUS, and known AF with or without prior stroke. We followed patients with ESUS prospectively for the primary outcome of recurrent ischemic stroke, incident AF, or both. Results We enrolled 203 patients from three centers: 103 patients without AF (35 healthy controls, 15 with lacunar strokes, 53 with ESUS) and 100 patients with AF (50 with and 50 without prior stroke). Patients with ESUS had significantly higher atrial fibrosis (15.0 ± 6.2%) compared to healthy controls (8.1 ± 7.9%; <0.0001) and compared to lacunar stroke patients (10.8 ± 8.4; p = 0.02), but had comparable fibrosis to patients with AF with (17.9 ± 11.4%) or without prior stroke (16.6 ± 9.2%; p = NS for both). Over a mean follow‐up of 19 months, nine of 53 patients (16.9%) with ESUS experienced the combined primary outcome, which included six patients (11.3%) with recurrent ischemic stroke and five patients with incident AF (9.4%). Patients with ESUS with fibrosis ≥12% had a higher proportion of the combined outcome: 25.0% vs. 4.8%; p = 0.039. Conclusions Patients with ESUS demonstrate atrial fibrosis comparable to that seen in AF. Atrial fibrosis ≥12% was associated with recurrent stroke, incident AF or both. This subgroup of ESUS patients may benefit from anticoagulation for secondary prevention of ischemic stroke.

Cardiac magnetic resonance imaging (MRI) has revealed fibrosis in embolic stroke of undetermined source (ESUS) patients comparable to levels seen in atrial fibrillation (AFib). We used computational modeling to understand the absence of arrhythmia in ESUS despite the presence of putatively pro-arrhythmic fibrosis. MRI-based atrial models were reconstructed for 45 ESUS and 45 AFib patients. The fibrotic substrate's arrhythmogenic capacity in each patient was assessed computationally. Reentrant drivers were induced in 24/45 (53%) ESUS and 22/45 (49%) AFib models. Inducible models had more fibrosis (16.7±5.45%) than non-inducible models (11.07±3.61%; P<0.0001); however, inducible subsets of ESUS and AFib models had similar fibrosis levels (P=0.90), meaning the intrinsic pro-arrhythmic substrate properties of fibrosis in ESUS and AFib are indistinguishable. This suggests some ESUS patients have latent pre-clinical fibrotic substrate that could be a future source of arrhythmogenicity. Thus, our work prompts the hypothesis that ESUS patients with fibrotic atria are spared from AFib due to an absence of arrhythmia triggers.

Background: Unexpected high levels of atrial fibrosis are found in individuals with no history of atrial fibrillation (AF). The temporal behavior of atrial fibrosis in this population is still unknown. We sought to investigate the progression and predictors of atrial fibrosis in non-AF individuals.Methods: Non-AF individuals at baseline who underwent late gadolinium enhancement magnetic resonance imaging (LGE-MRI) for assessment of left atrial (LA) fibrosis at least twice were retrospectively included in this study. The incidence of AF was assessed using review of medical records.Results: In 42 non-AF patients (15 females, 65.9 ± 8.6 years old), all patients had a detectable level of LA fibrosis at baseline, ranging from 4.5% to 28.8%, with a mean of 12.9 ± 5.9%. LA fibrosis in the second LGE-MRI was significantly higher in all patients compared to the first measurement (mean value of 12.9 ± 5.9% vs.17.34 ± 6.8%; p < .05). Congestive heart failure was a significant clinical predictor of atrial fibrosis progression. The seven patients (16.6%) who developed new-onset AF during follow-up showed a significantly higher degree of LA fibrosis on their second MRI, compared to individuals who stayed in sinus rhythm (20.5 ± 6.9% vs. 16.7 ± 6.7%, p < .05). Conclusion:Atrial fibrotic remodeling is a dynamic process that is progressively increasing in non-AF patients, accentuated by congestive heart failure. The higher extent of LA remodeling observed in patients who developed AF could highlight either the fact that AF is an expression of a highly dynamic left atrial substrate, or that remodeling processes are accelerated by AF.